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arXiv 1805.07528q-bio.NC
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给定参数变化的细胞函数:Hodgkin-Huxley模型中的兴奋性

Cellular function given parametric variation: excitability in the Hodgkin-Huxley model

Hillel Ori, Eve Marder, Shimon Marom

摘要:

尽管控制细胞功能的多个相互作用过程的关键参数的值存在相当大的变化,但如何在细胞中维持可靠的生理功能?在这里,我们使用经典的霍奇金-赫胥黎制定的鱿鱼巨轴突动作电位,提出一个可能的方法来解决这个问题。虽然完整的Hodgkin-Huxley模型对许多参数独立发生的波动非常敏感,但结果实际上是由这些参数沿两个生理维度的简单组合决定的:结构和动力学(表示为$S$和$K$)。结构参数描述细胞的性质,包括其电容和其离子通道的密度。动力学参数是描述电压依赖性电导的打开和关闭的参数。参数波动对系统动力学的影响,在Hodgkin-Huxley模型的高维表示中看似复杂,但在$S-K$平面内检查时是容易处理的。我们证明,缓慢失活,一个普遍存在的活性依赖性功能的离子通道,是一个强大的局部稳态控制机制,稳定兴奋性之间的结构和动力学参数的变化。

英文摘要:

How is reliable physiological function maintained in cells despite considerable variability in the values of key parameters of multiple interacting processes that govern that function? Here we use the classic Hodgkin-Huxley formulation of the squid giant axon action potential to propose a possible approach to this problem. Although the full Hodgkin-Huxley model is very sensitive to fluctuations that independently occur in its many parameters, the outcome is in fact determined by simple combinations of these parameters along two physiological dimensions: Structural and Kinetic (denoted $S$ and $K$). Structural parameters describe the properties of the cell, including its capacitance and the densities of its ion channels. Kinetic parameters are those that describe the opening and closing of the voltage-dependent conductances. The impacts of parametric fluctuations on the dynamics of the system, seemingly complex in the high dimensional representation of the Hodgkin-Huxley model, are tractable when examined within the $S-K$ plane. We demonstrate that slow inactivation, a ubiquitous activity-dependent feature of ionic channels, is a powerful local homeostatic control mechanism that stabilizes excitability amid changes in structural and kinetic parameters.

机构、总结、中文摘要均由AI分析而来,可能存在错误,请以论文正文为准。

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